000841567 001__ 841567 000841567 005__ 20210129232035.0 000841567 0247_ $$2doi$$a10.1021/jacs.7b10343 000841567 0247_ $$2pmid$$apmid:29235346 000841567 0247_ $$2WOS$$aWOS:000422813300060 000841567 0247_ $$2altmetric$$aaltmetric:33346387 000841567 037__ $$aFZJ-2017-08605 000841567 082__ $$a540 000841567 1001_ $$0P:(DE-Juel1)151182$$aBarz, Bogdan$$b0$$eCorresponding author$$ufzj 000841567 245__ $$aPathways of amyloid-β aggregation depend on oligomer shape 000841567 260__ $$aWashington, DC$$bAmerican Chemical Society$$c2018 000841567 3367_ $$2DRIVER$$aarticle 000841567 3367_ $$2DataCite$$aOutput Types/Journal article 000841567 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1517573247_13746 000841567 3367_ $$2BibTeX$$aARTICLE 000841567 3367_ $$2ORCID$$aJOURNAL_ARTICLE 000841567 3367_ $$00$$2EndNote$$aJournal Article 000841567 520__ $$aOne of the the main research topics related to Alzheimer’s disease is the aggregation of the amyloid-β peptide, which was shown to follow different pathways for the two major alloforms of the peptide, Aβ40 and the more toxic Aβ42. Experimental studies emphasized that oligomers of specific sizes appear in the early aggregation process in different quantities and might be the key toxic agents for each of the two alloforms. We use transition networks derived from all-atom molecular dynamics simulations to show that the oligomers leading to the type of oligomer distributions observed in experiments originate from compact conformations. Extended oligomers, on the other hand, contribute more to the production of larger aggregates thus driving the aggregation pro cess. We further demonstrate that differences in the aggregation pathways of the two Aβ alloforms occur as early as during the dimer stage. 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